Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

After about age 20, we may have all the insulin-producing beta cells we're ever going to get. So if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It's not just any fat; it's saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a result of free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren't just based on test tube studies. If researchers have infused fat into people's blood streams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by "defects in both insulin secretion and insulin action," and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics, so their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, "insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat]." This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. "[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action," contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn't just toxic to the pancreas. The fats found predominantly in meat and dairy--chicken and cheese are the two main sources in the American diet--are considered nearly "universally toxic." In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It's not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, "may contribute to the development of insulin resistance and its clinical consequences." After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn't develop lung cancer, everyone who eats a lot of saturated fat doesn't develop diabetes--there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.